S5) Diabetes Flashcards
Describe four different functions of insulin in the body
- Stimulates uptake of glucose into liver, muscle and adipose tissue
- Inhibits gluconeogenesis
- Inhibits glycogenolysis
- Promotes fat uptake
What are the six main insulin categories?
- Ultrafast acting
- Rapid acting (bolus → before meals)
- Short acting
- Intermediate acting
- Long acting (basal - bolus → keeps steady levels)
- Very long acting
How is insulin absorbed and administered?
Absorption into blood stream via subcutaneous injection
→ upper arms, thighs, buttocks, abdomen
Provide an example of an ultra fast acting insulin
Aspart (FiAsp)
Provide two examples of rapid acting insulins
- Humalog
- Novorapid
Describe the following for rapid acting insulins:
- Onset
- Administer
- Peak
- Duration
- Onset: rapid (5-15 minutes)
- Administer: inject just before eating
- Peak: ~60 minutes
- Duration: 4-6 hours
Provide two examples of short acting insulins
- Actrapid
- Humulin S
Describe the following for short acting insulins:
- Onset
- Administer
- Peak
- Duration
- Onset: 30-60 minutes
- Administer: inject at least 15-30 minutes before eating several times daily to cover meals
- Peak: 2-3 hours
- Duration: 8-10 hours
Provide an example of intermediate acting insulins
Humulin I
Describe the following for intermediate acting insulins:
- Onset
- Peak
- Duration
- Onset: 2-4 hours (slower)
- Peak: 4-8 hours
- Duration: 12-20 hours
Provide three examples of long and very long acting insulins
- Glargine
- Detemir
- Degludec
Describe the following for long and very long acting insulins:
- Onset
- Duration
- Onset: 2-66 hours (slow)
- Duration: up to 24 hours (very long up to 50+ hours)
Identify five adverse effects of insulin
- Hypoglycaemia
- Hyperglycaemia
- Lipodystrophy (lipohypertrophy / lipoatrophy) → lipid build up at sight of injection
- Painful injections
- Insulin allergies
How does one treat Type II diabetes?
- Lifestyle +
- Non-insulin therapies e.g. α- Glucosidase inhibitors, SGLT2s :1st step: metafotmin
- 2; SGLT2 inhibitors (stop glucose reabsorption in kidneys)*
- Non pharmacologic methods (bariatric surgery and very low calorie diets)
What are the key challenges for patients with Type 2 diabetes in terms of patient adherence and quality of life?
- Weight gain (or fear of weight gain)
- Risk of hypoglycaemia (or perceived risk)
What is the NICE target for Hbac1 for treating patients with Type II Diabetes?
In general target for all is HbA1c 6.5 to 7.5%
- HbA1c 6.5%: Diet and first 2 treatment steps
- HbA1c 7.5%: Beyond this or if at risk of severe hypoglycaemia
Describe the four effects of metformin (biguanides) on the body
- ↓ insulin resistance leading to increased glucose by tissues
- ↓ hepatic gluconeogenesis
- Limits weight gain by surpassing appetite
- ↓ CVS events
What are the side effects of metformin?
- GI symptoms (nausea, loose stools, diarrhoea)
- Vitamin B12 deficiency (uncommon)
- Lactic acidosis (rare)
Describe the two effects of sulphonylureas on the body
- Stimulate beta cell to release insulin
- blocks ATP dependent K channels
- ↓ Microvascular risk
What are the side effects of sulphonylureas?
- Weight gain → more insulin means more glucose being turned into fat
- Hypoglycaemia (don’t give to people with hepatic or renal failure)
- gi upset
Describe the effects of acarbose, an α glucosidase inhibitor, on the body
Acarbose Inhibits the breakdown of carbohydrates to glucose by blocking action of the enzyme α glucosidase
What are the side effects of acarbose?
Predictable:
- Flatulence
- Loose stools
- Diarrhoea
Describe the 3 effects of glitazones on the body
- ↑ insulin sensitivity in muscle and adipose tissue
- ↓ hepatic glucose output
- they interfere with gene transcription
- Bind to and activate 1/more peroxisome proliferator-activated receptors (PPARs)
Describe the side effects for the following glitazone drugs:
- Rosiglitazone
- Pioglitazone
- Rosiglitazone – heart failure due to fluid retention
- Pioglitazone – weight gain, fluid retention, heart failure, effects on bone metabolism and bladder cancer
Describe the mechanism and use of glucagon like peptide 1 therapies
- Mechanism: alternative hormone system influencing glucose metabolism
- Use: high glucose in Type II diabetes due to insufficient release of insulin and over production of glucagon
subcutaneous injection
Identify three drugs used in GLP 1 therapy
- Exenatide
- Liraglutide
- Lixisenatide
Describe the physiological effects of GLP 1 therapies on the pancreas
- Increase insulin secretion from the beta cells
- Decreases production of glucagon from alpha cells
What are the side effects of GLP 1 agonists?
- GI symptoms (nausea, loose stools, diarrhoea)
- Gastro oesophageal reflux
- Hypoglycaemia (low risk)
- Pancreatitis and pancreatic carcinoma (possible)
Identify a contra-indication for GLP 1 agonists
Avoid if eGFR < 30ml/min
Provide four examples of Gliptins (/ DPP-4 inhibitors)
- Sitagliptin
- Vildagliptin
- Saxagliptin
- Linagliptin
Describe the effects of gliptins on the body
Inhibits DPP-4 activity by increasing postprandial active GLP-1 concentrations, prevents breakdowns of insulin so increased plasma insulin levels
→ glucose dependent
→ surpasses appetite
What are the side effects of gliptins?
- GI symptoms (nausea, loose stools, diarrhoea)
- Pancreatitis
- Hypoglycaemia (low risk)
- HbA1c reduction (modest)
When are glifozins used and how do they work?
Glifozins can be used for patients with Type I and Type II diabetes as add on therapy (started to give to people with CVD risk patients)
SGLT-2 inhibitors
→ reduce glucose reabsorption in proximal tubule so increase glucose urinary excretion
Provide three examples of glifozins
- Dapagliflozin
- Canagliflozin
- Empagliflozin
What are the side effects of glifozins?
- Lower urinary tract symptoms (increased risk)
- Polyuria
- Hypoglycaemia (low risk)
difference between measuring glucose and HbA1c levels
→ glucose measures immediate glucose in the body
→ HbA1c shows percentages of red blood cells that are gylcated (sugar coated)
diabetic ketoacidosis (bichemical triad)
→ low insulin so glucose isn’t being stored in cells and they can’t use it
-→ body breaks down ketones to use for energy
TRIAD:
- hyperglycemia
- ketonaemia
- acidosis
if someone is suspected with diabetic ketoacidosis what tests will you do?
→ blood glucose > 11 mmol/L BAD
→ test for ketones in URINE
→ test blood for acidosis (HC03 levels)
why can’t you give insulin as a tablet?
→ it is a protein so the body will break it down before it can act appropriately
→ we need slow absorption
what can you use to slow down the absorption of insulin (not used as much now)
→ protamine and/or Zinc with natural (bovine/porcine) insulin
what medication causes insulin dose to be increased
systemic steroids
steroids can cause insulin resistance
what is diabulimia
- person with type 1 diabetes stops taking insulin to control weight
- eating disorder
drug interactions of metformin
- ACEi (can increase effect of metformin)
- NSAIDS -. Lactic acidosis
- loops and thiazide like diuretics (increases glucose so oppose metformin)
overall what type of agents should you avoid giving hypoglycaemic agents with
→ other hypoglycaemic agents as you will result dropping glucose levels too low
→ some loop diuretics and thiazide like diuretics can increase glucose levels in the body
Role of glp-1
why would It be difficult to have a single pill that contains multiple drugs in it
→ if you wanted to slightly change dose it would be hard to manufacture and expensive
but it would be easy adherence for the patient
how will the dose of insulin change with people who have renal impairment
their kidneys don’t work as well
reduced insulin clearance
more plasma insulin
so less dosage of insulin needed
